The distally based anterolateral thigh flap has been used for coverage of soft-tissue defects of the knee and upper third of the leg. This flap is based on the septocutaneous or musculocutaneous perforators derived from the lateral circumflex femoral system. The purpose of this study was to examine the results of anatomical variations of the descending branch of the lateral circumflex femoral artery and the retrograde blood pressure of the descending branch of the lateral circumflex femoral artery so that the surgical technique for raising and transferring a distally based anterolateral thigh flap to the knee region could be improved. The authors have actually used this flap in three cases. In 11 thighs of six cadavers, the descending branch of the lateral circumflex femoral artery had a rather consistent connection with the lateral superior genicular artery or profunda femoral artery in the knee region. The pivot point, located at the distal portion of the vastus lateralis muscle, ranges from 3 to 10 cm above the knee. In their three cases, the maximal flap size was 7.0 x 16.0 cm and was harvested safely, without marginal necrosis. The mean pedicle length was 15.2 +/- 0.7 cm (range, 14.5 to 16 cm). The average proximal and distal retrograde blood pressure of the descending branch of the lateral circumflex femoral artery was also studied in another 11 patients, and the anterolateral thigh flap being used for reconstruction of head and neck defects showed 58.3 and 77.7 percent of proximal antegrade blood pressure, respectively. The advantages of this flap include a long pedicle length, a sufficient tissue supply, possible combination with fascia lata for tendon reconstruction, and favorable donor-site selection, without sacrifice of major vessels or muscles.

Cordycepin (3'-deoxyadenosine), a pure compound of Cordyceps sinensis, has been illustrated with anti-tumor effects. In the present study, the apoptotic effect of cordycepin on OEC-M1, a human oral squamous cancer cell line, was investigated by morphological observations, cell viability assay, annexin V-FITC analysis and flow cytometry methods. Results demonstrated that the number of rounded-up cell increased as treatment duration of cordycepin (100 microM) increased from 3 to 48 h, and the plasma membrane blebbing could be observed after 12 h treatment. In cell viability assay, cell surviving rate significantly decreased as the dosage and duration of cordycepin treatment increased (P < 0.05). Moreover, phosphatidylserine flipping on cell membrane could be detected with 3, 6 and 12 h cordycepin treatment, which indicated an early apoptotic phenomenon. Furthermore, cell cycle studies illustrated that the percentage of G1 phase cell declined as the dosages of cordycepin increased (10 microM to 5 mM), while the percentages of G2M and subG1 phase cell increased (P < 0.05) in 12, 24 and 48 h cordycepin treatment. These results further confirmed the apoptotic event. In conclusion, cordycepin significantly induced cell apoptotsis in OEC-M1 human oral squamous cancer cells.

The p38 MAPKs play important roles in the regulation of balance between cell survival and cell death on the development of various cancers. However, the roles of p38 MAPKs regulating apoptotic effects on Leydig tumor cells remain unclear. In the present study, we showed that cordycepin (3′-deoxyadenosine) selectively induced apoptosis in MA-10 mouse Leydig tumor cells through regulating the p38 MAPK and PI3K/AKT signaling pathways. Cordycepin reduced viability in MA-10, TM4, and NT2/D1 cells, but not cause cell death of primary mouse Leydig cells on moderate concentration. Cordycepin increased reactive oxygen species (ROS) levels, which is associated with the induction of apoptosis as characterized by positive Annexin V binding, activation of caspase-3, and cleavage of PARP. Inhibition of p38 MAPKs activity by SB203580 significantly prevented cordycepin-induced apoptosis in MA-10 cells. Co-treatment with wortmannin or the autophagy inhibitor 3-methyladenine (3-MA) elevated levels of apoptosis in cordycepin-treated MA-10 cells. Moreover, cordycepin activated p53, p21 and TGFß; and downregulated CDK2. The antitumour activity of cordycepin-treated MA-10 cells was significantly distinct in severe combined immunodeficiency (SCID) mice in vivo. These results suggested that cordycein is a highly selective treatment to induce MA-10 cells apoptosis via p38 MAPKs signaling.